This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. This project seeks to study the mechanism of action of antillatoxin on recombinant NMDA receptors using patch-clamp and intracellular calcium measurements. Antillatoxin, a potent neurotoxic isolated from cyanobacterium Lyngbya majuscula, is provided by my colleague Dr. David Horgen. I believe that my expertise in patch-clamp electrophysiology of neurotransmitter receptors (nAChR, NMDA receptors, Kainate receptors and glycine receptors) and fluorescence techniques (MS and Ph.D studies) made me suitable to successfully conduct the proposed research. I obtained my postdoctoral training with Dr. George Hess at Cornell University and continued to conduct research there for a few more years. Specific Aim 1: To explore the mechanism underlying the acute toxicity of antillatoxin through the NMDA receptors overexpressed in HEK 293 cells Specific Aim 2: To study the mechanism of action of intracellular sodium on the recombinant NMDA receptors overexpressed in HEK 293 cells.